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Effect of Energy Substrates on Protein Degradation in Isolated Small Intestinal Enterocytes From Rats

Mohsen T. Saberi, BSc^*, Sarah A. Stewart^*, Myriam Annette, BSc^*, Andrew L. Knowles, MSc^*, Didier Attaix, PhD and Sue E. Samuels, PhD^*

From ^* Food, Nutrition and Health, University of British Columbia, Vancouver, British Columbia, Canada; and Human Nutrition Unit, INRA de Theix, Ceyrat, France

Correspondence: Sue E. Samuels, PhD, 2357 Main Mall, McMl 223, Food, Nutrition and Health, The University of British Columbia, Vancouver, BC, V6T 1Z4 Canada. Electronic mail may be sent to ssamuels{at}interchange.ubc.ca.

Background: Nutrients affect small intestinal protein mass and metabolism, but studies on the effect of nutrients on small intestinal protein degradation are very limited due to a lack of a proper method. The objectives of this study were to establish a method to directly estimate protein degradation in isolated enterocytes from rats and to test the effect of energy substrates on protein degradation. Methods: Male Sprague-Dawley rats (150–200 g, n 8 per treatment) were used. Cell viability, tyrosine release as an indicator of protein degradation, and the effect of osmolarity, 50 mmol/L glucose, 20 mmol/L β-hydroxybutyrate, 4.7 mmol/L butyrate, and 30 mmol/L glutamine on protein degradation were measured. Results: The average viability of enterocytes at time 30 minutes was 85.8% (range, 81%–94%). Tyrosine release was linear over the course of experiments, indicating constant protein degradation (R² = 0.9943; p < .05). Osmolarity, glucose, and glutamine had no effect on protein degradation in isolated enterocytes. β-Hydroxybutyrate significantly decreased it (–16%; p < .05), whereas butyrate slightly increased it (+5%; p < .05). Conclusions: A high viability and constant protein degradation indicate a successful establishment of a method to estimate protein degradation in isolated small intestinal enterocytes from rats. The large effect of β-hydroxybutyrate suggests a potential positive role for ketone bodies to limit the loss of small intestinal protein mass by decreasing protein degradation.

Journal of Parenteral and Enteral Nutrition, Vol. 30, No. 6, 497-502 (2006)
DOI: 10.1177/0148607106030006497


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